Connective tissue deposition or collagen remodeling during the maturation phase depends on continued collagen synthesis in the presence of collagen destruction. Collagenases and matrix metalloproteinases in the wound assist in the removal of excess collagen, although synthesis of new collagen persists. Tissue inhibitors of metallo-proteinases limit these collagenolytic enzymes so that a balance exists between formation of new collagen and removal of old collagen.
During remodeling, collagen becomes more organized. Fibronectin gradually disappears, and hyaluronic acid and glycosaminoglycans are replaced by proteogly-cans. Type III collagen is replaced by type I collagen. Water is resorbed from the scar. These events allow collagen fibers to lie closer together, facilitating collagen cross-linking and ultimately decreasing scar thickness. Intramolecular and intermolecular collagen cross-links result in increased wound bursting strength. Remodeling begins approximately 21 d after injury, when the net collagen content of the wound is stable and may continue indefinitely.
The tensile strength of a wound is a measurement of its load capacity per unit area. The bursting strength of a wound is the force required to break a wound regardless of its dimension. Bursting strength varies with skin thickness. Peak tensile strength of a wound occurs approximately 60 d after injury. A healed wound reaches only approximately 80% of the tensile strength of unwounded skin. The roles of topical manganese, calcium, zinc, and ascorbic acid dressings in the treatment of chronic wounds and positive steps in tensile strength remain to be elucidated.
The zinc- and calcium-dependent family of proteins called the matrix metallo-proteinases is collectively responsible for the degradation of the extracellular matrix. Members of this family, such as the collagenases, stromelysins, and the gelatinases, are involved in the routine tissue remodeling processes, such as wound healing, embryonic growth, and angiogenesis. Imbalance between the active enzymes and their natural inhibitors leads to the accelerated destruction of connective tissue associated with the pathology of diseases such as rheumatoid arthritis and osteoar-thritis (Figure 10.1). Micronutrients, and particularly trace elements, again, are constituents of complex physiologic processes dealing with all of these stages.
Angiogenesis (via platelet inhibition) launches the collagen/extracellular matrix interaction that initiates the release of clotting factors, growth factors, and cytokines.
In short, following this period of hemostasis, neutrophils, and the business of phagocytosis to remove foreign materials, bacteria and damaged tissue move to the forefront. Macrophages help with the engulfment of foreign materials and release additional growth
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